Добавил:

Sekretar kiopkiopkiop18@yandex.ru t.me/Prokururor I Вовсе не секретарь, но почту проверяю Опубликованный материал нарушает ваши авторские права? Сообщите нам.

Вуз:

Ростовский Государственный Медицинский Университет

Предмет:

Медицина общая

Файл:

Книга_3774_Библиотеки_им_академика_М_И_Перельмана

.pdf

Скачиваний:

Добавлен:

02.09.2026

Размер:

20 Мб

Скачать

☆

<<< < Предыдущая 1 2 3 4 5 6 7 89 / 509 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 > Следующая >>>

https://t.me/medicina_free

Mechanisms oftheVulnerable Atherosclerotic Plaque andImaging

future major adverse cardiovascular events (MACE) [87, 88]. However, IVUS is not able to detect thin-brous caps (<65μm) due to its inferior spatial resolution [89].

3.8.2 Optical Coherence Tomography (OCT)

Optical coherence tomography (OCT) uses near-infrared light to produce images with a superior spatial resolution of 10–30μm. This allows OCT to measure the brous-cap thickness [90], macrophage density [91], collagen and smooth muscle cells content [92], characterise plaques as brous, brocalcic, and lipid-rich plaques [93], and identify neovessels, cholesterol crystals, ruptures and thrombi [94, 95]. The correspondence between plaque and OCT features can be seen in Table3.3 and Fig.3.7. However, as OCT has a penetration of approximately 1.5mm, it is not able to image the deeper plaque and estimate the size of the necrotic core or identify positive remodeling. Additionally, the OCT rays can be attenuated by blood and so OCT requires a blood-free eld unlike IVUS.It can also be difcult to differentiate calcied plaques from necrotic core as they both appear as signal poor areas with the only difference being the delineation of their borders (sharply delineated borders in calcied plaque, poorly delineated in necrotic core) [96].

Plaque features derived from OCT including OCT-TCFA, and thinner brous cap thickness have been associated with lesions causing acute MI and NSTEMI/ Unstable angina, as opposed to stable angina lesions [97]. OCT derived features including lipid-rich plaque, thin brous cap, TCFA and brous cap macrophage density have been associated with positive remodeling [98].

Table 3.3 Correspondence of plaque features with optical coherence tomography (OCT)

Plaque features on optical coherence tomography (OCT) Plaque features Appearance on OCT

Fibrous plaque Homogenous signal, highly backscattering signal Calcied plaque Signal poor area with sharply delineated borders Fibrocalcic

plaque Fibrous cap Signal-rich area overlying a signal poor area Necrotic core Signal-poor area with poorly delineated borders covered by a brous cap OCT-TCFA Necrotic core with overlying brous cap with thickness <65μm Macrophages Signal-rich punctate regions at border of brous cap and necrotic zone Cholesterol

crystals Red thrombus Lower signal (than white thrombus), <250μm half-width (distance from max

White thrombus Higher signal, >250μm half-width Intimal

vasculature

Tearney, Regar [95], Kume, Akasaka [90]

Fibrous tissue+calcication (both as described above)

Linear regions of high signal intensity

signal intensity to half-signal intensity)

Signal-poor, sharply delineated in multiple contiguous frames

https://t.me/medicina_free

K. Rana et al.

Fig. 3.7 Optical coherence tomography correlation with histology. (a) Fibrotic plaque shows a high signal and low attenuation. (b) A calcied plaque shows calcied regions (‡) that have a poor signal with sharply delineated borders. (c) The lipid rich plaque has a lipid core (∗) that has a diffuse border and high light attenuation. The thickness of the overlying brotic cap can be measured; in this case a thick cap (>200μm) is present. (Reprinted from Bezerra, Costa [111])

3 Mechanisms oftheVulnerable Atherosclerotic Plaque andImaging

https://t.me/medicina_free

Table 3.4 The strengths and limitations of intravascular ultrasound and optical coherence tomography to image vulnerable plaque features

Intravascular ultrasound and optical coherence tomography for imaging of vulnerable plaque features

Resolution Penetration Strengths Limitations

•

Intravascular ultrasound

Optical coherence tomography

70–200μm axial 200–400μm lateral

10–30μm 1.5mm •

5–10mm •

Fibrous tissue,

bro-fatty, calcium dense, necrotic core

•

Plaque burden

(PAV)

• Lumen area

• Positive remodelling VH-TCFA

• Fibrous cap

thickness

• Collagen content

• Macrophages

• Neovessels

• Plaque rupture

• Thrombus

• Can detect plaque

erosion

Fibrous cap thickness

(<65μm)

Flush required as blood

• attenuates light

• Limited penetration depth to image deeper plaque, estimate necrotic core size, positive remodelling

•

Poor discrimination

between calcied areas and lipid core

Due to its spatial resolution of 10–30μm, OCT is unable to image individual cells and subcellular processes implicated in atherosclerosis and coronary events (Table3.3). μOCT is a further development from the standard OCT with a signicantly superior resolution of 1-μm. μOCT has shown potential to visualize processes including leukocyte adhesion and diapedesis, clot morphologies, cholesterol crystals, microcalcications, brin strand formation, ECM production, and quantify macrophage distribution [94, 99, 100]. Visualising these subcellular processes invivo may help provide a new level of insight to characterize and identify vulnerable plaques (Table3.4).

3.8.3 Intravascular Molecular Imaging

Intravascular near-infrared uorescence (NIRF) involves the use of targeted molecular contrast agents to highlight via uorescence certain processes implicated in plaque rupture. The advantage of near-infrared light includes lower attenuation of light rays through blood and lower autouorescence [101]. Studies in this arena have included using indocyanine green to highlight endothelial abnormalities [101], and mapping arterial inammation with the use of a contrast agent that highlights the inammation regulated cysteine protease [102]. However, many of the contrast agents used in NIRF have not been approved for use in humans. Alternatively, near- infrared autouorescence (NIRAF) can detect uorescence from naturally

https://t.me/medicina_free

K. Rana et al.

occurring molecules, negating the need for contrast agents. NIRAF has been safely used in humans. Promisingly, a signicantly higher maximum NIRAF signal was associated with vulnerable plaques including OCT-delineated TCFA and plaque rupture cases [103]. However, further studies are needed to understand the molecular sources of NIRAF and its clinical signicance.

3.9 Conclusion: Vulnerable Plaques andVulnerable Patients

Post-mortem studies and subsequent imaging studies have clearly demonstrated the association of acute cardiovascular events with certain forms of plaque disruption [33, 95]. In approximately two thirds of all cases, plaque characteristics were associated with thin-capped atheroma along with a large necrotic core, suggesting the preceding destabilization. Plaque erosion accounts for the most of the of remaining events, but is less well understood, but can be imaged using OCT.Many attempts so far have been made to diagnose and predict events based on plaque characteristics that could be associated with a high-risk plaque. Nevertheless, this has been less successful than hoped, illustrated by the relatively disappointing results of the PROSPECT trial [104].

It seems evident that at least another decade of research is needed to develop better tools to assess high-risk plaques in coronary, carotid and peripheral arterial disease. In the meanwhile, another important realisation is that many chronic diseases, including atherosclerotic disease, are helped by taking a more holistic systemsbased approach. This involves detecting the patient at high risk of cardiovascular events by taking into account variables based on blood biomarkers and myocardial vulnerability, in addition to the vulnerable plaque [33].

References

1. Barquera S, Pedroza-Tobias A, Medina C, Hernandez-Barrera L, Bibbins-Domingo K, Lozano

R, etal. Global overview of the epidemiology of atherosclerotic cardiovascular disease. Arch

Med Res. 2015;46:328–38.

2. Davies MJ, Thomas A.Thrombosis and acute coronary-artery lesions in sudden cardiac isch-

aemic death. N Engl J Med. 1984;310:1137–40.

3. Friedman M.The pathogenesis of coronary plaques, thromboses, and hemorrhages: an evalua-

tive review. Circulation. 1975;52:III34–40.

4. Burke AP, Farb A, Malcom GT, Liang YH, Smialek J, Virmani R. Coronary risk factors

and plaque morphology in men with coronary disease who died suddenly. N Engl J Med.

1997;336:1276–82.

5. Virmani R, Kolodgie FD, Burke AP, Farb A, Schwartz SM.Lessons from sudden coronary

death: a comprehensive morphological classication scheme for atherosclerotic lesions.

Arterioscler Thromb Vasc Biol. 2000;20:1262–75.

6. Bentzon JF, Otsuka F, Virmani R, Falk E.Mechanisms of plaque formation and rupture. Circ

Res. 2014;114:1852–66.

https://t.me/medicina_free

Mechanisms oftheVulnerable Atherosclerotic Plaque andImaging

7. Bennett MR, Evan GI, Schwartz SM.Apoptosis of human vascular smooth muscle cells derived

from normal vessels and coronary atherosclerotic plaques. J Clin Invest. 1995;95:2266–74.

8. Bennett MR.Apoptosis of vascular smooth muscle cells in vascular remodelling and athero-

sclerotic plaque rupture. Cardiovasc Res. 1999;41:361–8.

9. Zohlnhofer D, Richter T, Neumann F, Nuhrenberg T, Wessely R, Brandl R, etal. Transcriptome

analysis reveals a role of interferon-gamma in human neointima formation. Mol Cell. 2001;7:1059–69.

10. Ovchinnikova O, Robertson AKL, Wågsäter D, Folco EJ, Hyry M, Myllyharju J, etal. T-cell

activation leads to reduced collagen maturation in atherosclerotic plaques of Apoe(−/−) mice. Am J Pathol. 2009;174:693–700.

11. Shah PK.Mechanisms of plaque vulnerability and rupture. J Am Coll Cardiol. 2003;41:15S–22S.

12. Schoenhagen P, Ziada KM, Kapadia SR, Crowe TD, Nissen SE, Tuzcu EM.Extent and direc-

tion of arterial remodeling in stable versus unstable coronary syndromes: an intravascular ultrasound study. Circulation. 2000;101:598–603.

13. Ye S, Humphries S, Henney A. Matrix metalloproteinases: implication in vascular matrix

remodelling during atherogenesis. Clin Sci (Lond). 1998;94:103–10.

14. Liu P, Sun M, Sader S.Matrix metalloproteinases in cardiovascular disease. Can J Cardiol.

2006;22:25B–30B.

15. von Birgelen C, Klinkhart W, Mintz GS, Papatheodorou A, Herrmann J, Baumgart D, etal.

Plaque distribution and vascular remodeling of ruptured and nonruptured coronary plaques in the same vessel: an intravascular ultrasound study invivo. J Am Coll Cardiol. 2001;37:1864–70.

16. Falk E, Shah PK, Fuster V.Coronary plaque disruption. Circulation. 1995;92:657–71.

17. Davies MJ, Richardson PD, Woolf N, Katz DR, Mann J.Risk of thrombosis in human athero-

sclerotic plaques: role of extracellular lipid, macrophage, and smooth muscle cell content. Br Heart J. 1993;69:377–81.

18. Felton CV, Crook D, Davies MJ, Oliver MF.Relation of plaque lipid composition and morphol-

ogy to the stability of human aortic plaques. Arterioscler Thromb Vasc Biol. 1997;17:1337–45.

19. Toschi V, Gallo R, Lettino M, Fallon JT, Gertz SD, Fernandez-Ortiz A, et al. Tissue factor

modulates the thrombogenicity of human atherosclerotic plaques. Circulation. 1997;95:594–9.

20. Camaré C, Pucelle M, Nègre-Salvayre A, Salvayre R. Angiogenesis in the atherosclerotic

plaque. Redox Biol. 2017;12:18–34.

21. Falk E.Pathogenesis of atherosclerosis. J Am Coll Cardiol. 2006;47:C7–12.

22. Virmani R, Narula J, Farb A.When neoangiogenesis ricochets. Am Heart J. 1998;136:937–9.

23. Kolodgie FD, Gold HK, Burke AP, Fowler DR, Kruth HS, Weber DK, etal. Intraplaque hemor-

rhage and progression of coronary atheroma. N Engl J Med. 2003;349:2316–25.

24. McCarthy MJ, Loftus IM, Thompson MM, Jones L, London NJ, Bell PR, etal. Angiogenesis

and the atherosclerotic carotid plaque: an association between symptomatology and plaque morphology. J Vasc Surg. 1999;30:261–8.

25. Modi R, Crotty TB, McCarthy P, Sheehan SJ, Mehigan D, Keaveny TV.Association between

plaque instability, angiogenesis and symptomatic carotid occlusive disease. Br J Surg. 2001;88:945–50.

26. Marathe S, Kuriakose G, Williams KJ, Tabas I.Sphingomyelinase, an enzyme implicated in

atherogenesis, is present in atherosclerotic lesions and binds to specic components of the subendothelial extracellular matrix. Arterioscler Thromb Vasc Biol. 1999;19:2648–58.

27. Guyton JR.Phospholipid hydrolytic enzymes in a ‘cesspool’ of arterial intimal lipoproteins:

a mechanism for atherogenic lipid accumulation. Arterioscler Thromb Vasc Biol. 2001;21: 884–6.

28. Sangiorgi G, Rumberger JA, Severson A, Edwards WD, Gregoire J, Fitzpatrick LA, etal.

Arterial calcication and not lumen stenosis is highly correlated with atherosclerotic plaque burden in humans: a histologic study of 723 coronary artery segments using nondecalcifying methodology. J Am Coll Cardiol. 1998;31:126–33.

29. Vliegenthart R, Oudkerk M, Hofman A, Oei HH, van Dijck W, van Rooij FJ, etal. Coronary cal-

cication improves cardiovascular risk prediction in the elderly. Circulation. 2005;112:572–7.

https://t.me/medicina_free

30. Ehara S, Kobayashi Y, Yoshiyama M, Shimada K, Shimada Y, Fukuda D, etal. Spotty calcica-

tion typies the culprit plaque in patients with acute myocardial infarction: an intravascular ultrasound study. Circulation. 2004;110:3424–9.

31. Kelly-Arnold A, Maldonado N, Laudier D, Aikawa E, Cardoso L, Weinbaum S. Revised

microcalcication hypothesis for brous cap rupture in human coronary arteries. Proc Natl Acad Sci U S A. 2013;110:10741–6.

32. Jia H, Abtahian F, Aguirre AD, Lee S, Chia S, Lowe H, etal. In vivo diagnosis of plaque ero-

sion and calcied nodule in patients with acute coronary syndrome by intravascular optical coherence tomography. J Am Coll Cardiol. 2013;62:1748–58.

33. Naghavi M, Libby P, Falk E, Casscells SW, Litovsky S, Rumberger J, etal. From vulnerable

plaque to vulnerable patient: a call for new denitions and risk assessment strategies: part I.Circulation. 2003;108:1664–72.

34. Virmani R, Burke AP, Farb A, Kolodgie FD.Pathology of the vulnerable plaque. J Am Coll

Cardiol. 2006;47:C13–8.

35. Kramer MC, Rittersma SZ, de Winter RJ, Ladich ER, Fowler DR, Liang YH, etal. Relationship

of thrombus healing to underlying plaque morphology in sudden coronary death. J Am Coll Cardiol. 2010;55:122–32.

36. Bentzon JF, Falk E. Plaque erosion: new insights from the road less travelled. Circ Res.

2017;121:8–10.

37. Mullick AE, Soldau K, Kiosses WB, Bell TA 3rd, Tobias PS, Curtiss LK.Increased endothelial

expression of Toll-like receptor 2 at sites of disturbed blood ow exacerbates early atherogenic events. J Exp Med. 2008;205:373–83.

38. Xu Y, Mintz GS, Tam A, McPherson JA, Iniguez A, Fajadet J, et al. Prevalence, distribu-

tion, predictors, and outcomes of patients with calcied nodules in native coronary arteries: a 3-vessel intravascular ultrasound analysis from Providing Regional Observations to Study Predictors of Events in the Coronary Tree (PROSPECT). Circulation. 2012;126:537–45.

39. Schurgin S, Rich S, Mazzone T.Increased prevalence of signicant coronary artery calcica-

tion in patients with diabetes. Diabetes Care. 2001;24:335–8.

40. Moreno PR, Murcia AM, Palacios IF, Leon MN, Bernardi VH, Fuster V, etal. Coronary com-

position and macrophage inltration in atherectomy specimens from patients with diabetes mellitus. Circulation. 2000;102:2180–4.

41. Yahagi K, Kolodgie FD, Lutter C, Mori H, Romero ME, Finn AV, etal. Pathology of human

coronary and carotid artery atherosclerosis and vascular calcication in diabetes mellitus. Arterioscler Thromb Vasc Biol. 2017;37:191–204.

42. Virmani R, Burke AP, Kolodgie F.Morphological characteristics of coronary atherosclerosis in

diabetes mellitus. Can J Cardiol. 2006;22:81B–4B.

43. Hong YJ, Jeong MH, Choi YH, Ko JS, Lee MG, Kang WY, etal. Plaque characteristics in

culprit lesions and inammatory status in diabetic acute coronary syndrome patients. JACC Cardiovasc Imaging. 2009;2:339–49.

44. Ramasamy R, Yan SF, Schmidt AM.Receptor for AGE (RAGE): signaling mechanisms in the

pathogenesis of diabetes and its complications. Ann N Y Acad Sci. 2011;1243:88–102.

45. Mathiesen EB, Bonaa KH, Joakimsen O. Echolucent plaques are associated with high

risk of ischaemic cerebrovascular events in carotid stenosis: the tromso study. Circulation. 2001;103:2171–5.

46. Aldemir E, Apaydin M, Varer M, Uluc E.Echolucency of carotid plaques and cerebrovascular

events. J Clin Ultrasound. 2012;40:399–404.

47. Sabetai MM, Tegos TJ, Nicolaides AN, Dhanjil S, Pare GJ, Stevens JM.Reproducibility of

computer-quantied carotid plaque echogenicity: can we overcome the subjectivity? Stroke. 2000;31:2189–96.

48. Elatrozy T, Nicolaides A, Tegos T, Grifn M.The objective characterisation of ultrasonic

carotid plaque features. Eur J Vasc Endovasc Surg. 1998;16:223–30.

49. Biasi GM, Sampaolo A, Mingazzini P, De Amicis P, El-Barghouty N, Nicolaides AN.Computer

analysis of ultrasonic plaque echolucency in identifying high risk carotid bifurcation lesions. Eur J Vasc Endovasc Surg. 1999;17:476–9.

K. Rana et al.

https://t.me/medicina_free

Mechanisms oftheVulnerable Atherosclerotic Plaque andImaging

50. Russell DA, Wijeyaratne SM, Gough MJ.Relationship of carotid plaque echomorphology to

presenting symptom. Eur J Vasc Endovasc Surg. 2010;39:134–8.

51. Devuyst G, Karapanayiotides T, Ruchat P, Pusztaszeri M, Lobrinus JA, Jonasson L, et al.

Ultrasound measurement of the brous cap in symptomatic and asymptomatic atheromatous carotid plaques. Circulation. 2005;111:2776–82.

52. Redgrave JN, Gallagher P, Lovett JK, Rothwell PM. Critical cap thickness and rupture in

symptomatic carotid plaques: the oxford plaque study. Stroke. 2008;39:1722–9.

53. de Bray JM, Baud JM, Dauzat M. Consensus concerning the morphology and the risk of

carotid plaques. Cerebrovasc Dis. 1997;7:289–96.

54. Watanabe Y, Nagayama M, Suga T, Yoshida K, Yamagata S, Okumura A, etal. Characterization of

atherosclerotic plaque of carotid arteries with histopathological correlation: vascular wall MR imaging vs. color Doppler ultrasonography (US). J Magn Reson Imaging. 2008;28:478–85.

55. Saba L, Caddeo G, Sanlippo R, Montisci R, Mallarini G.CT and ultrasound in the study of

ulcerated carotid plaque compared with surgical results: potentialities and advantages of multidetector row CT angiography. Am J Neuroradiol. 2007;28:1061–6.

56. ten Kate GL, van Dijk AC, van den Oord SC, Hussain B, Verhagen HJ, Sijbrands EJ, etal.

Usefulness of contrast-enhanced ultrasound for detection of carotid plaque ulceration in patients with symptomatic carotid atherosclerosis. Am J Cardiol. 2013;112:292–8.

57. Coli S, Magnoni M, Sangiorgi G, Marrocco-Trischitta MM, Melisurgo G, Mauriello A, etal.

Contrast-enhanced ultrasound imaging of intraplaque neovascularization in carotid arteries: correlation with histology and plaque echogenicity. J Am Coll Cardiol. 2008;52:223–30.

58. Huang PT, Huang FG, Zou CP, Sun HY, Tian XQ, Yang Y, etal. Contrast-enhanced sonographic

characteristics of neovascularization in carotid atherosclerotic plaques. J Clin Ultrasound. 2008;36:346–51.

59. Grant EG, Benson CB, Moneta GL, Alexandrov AV, Baker JD, Bluth EI, etal. Carotid artery

stenosis: gray-scale and Doppler US diagnosis—Society of Radiologists in Ultrasound Consensus Conference. Radiology. 2003;229:340–6.

60. Brinjikji W, Huston J 3rd, Rabinstein AA, Kim GM, Lerman A, Lanzino G.Contemporary

carotid imaging: from degree of stenosis to plaque vulnerability. J Neurosurg. 2016;124:27–42.

61. Wintermark M, Jawadi SS, Rapp JH, Tihan T, Tong E, Glidden DV, etal. High-resolution CT

imaging of carotid artery atherosclerotic plaques. Am J Neuroradiol. 2008;29(5):875–82.

62. Saba L, Lai ML, Montisci R, Tamponi E, Sanlippo R, Faa G, et al. Association between

carotid plaque enhancement shown by multidetector CT angiography and histologically validated microvessel density. Eur Radiol. 2012;22:2237–45.

63. Wintermark M, Arora S, Tong E, Vittinghoff E, Lau BC, Chien JD, etal. Carotid plaque com-

puted tomography imaging in stroke and nonstroke patients. Ann Neurol. 2008;64:149–57.

64. Miralles M, Merino J, Busto M, Perich X, Barranco C, Vidal-Barraquer F.Quantication and

characterization of carotid calcium with multi-detector CT-angiography. Eur J Vasc Endovasc Surg. 2006;32:561–7.

65. Saba L, Mallarini G.Fissured brous cap of vulnerable carotid plaques and symptomatic-

ity: are they correlated? Preliminary results by using multi-detector-row CT angiography. Cerebrovasc Dis. 2009;27:322–7.

66. Takaya N, Yuan C, Chu B, Saam T, Underhill H, Cai J, etal. Association between carotid

plaque characteristics and subsequent ischaemic cerebrovascular events: a prospective assessment with MRI—initial results. Stroke. 2006;37:818–23.

67. Chu B, Kampschulte A, Ferguson MS, Kerwin WS, Yarnykh VL, O’Brien KD, et al.

Hemorrhage in the atherosclerotic carotid plaque: a high-resolution MRI study. Stroke. 2004;35:1079–84.

68. Cai J, Hatsukami TS, Ferguson MS, Kerwin WS, Saam T, Chu B, etal. In vivo quantitative

measurement of intact brous cap and lipid-rich necrotic core size in atherosclerotic carotid plaque: comparison of high-resolution, contrast-enhanced magnetic resonance imaging and histology. Circulation. 2005;112:3437–44.

69. Gupta A, Baradaran H, Schweitzer AD, Kamel H, Pandya A, Delgado D, etal. Carotid plaque

MRI and stroke risk: a systematic review and meta-analysis. Stroke. 2013;44:3071–7.

https://t.me/medicina_free

70. Tarkin JM, Joshi FR, Rudd JH. PET imaging of inammation in atherosclerosis. Nat Rev

Cardiol. 2014;11:443–57.

71. Tawakol A, Migrino RQ, Bashian GG, Bedri S, Vermylen D, Cury RC, et al. In vivo

18F-uorodeoxyglucose positron emission tomography imaging provides a noninvasive measure of carotid plaque inammation in patients. J Am Coll Cardiol. 2006;48:1818–24.

72. Rudd JH, Warburton EA, Fryer TD, Jones HA, Clark JC, Antoun N, etal. Imaging athero-

sclerotic plaque inammation with [ Circulation. 2002;105:2708–11.

73. Folco EJ, Sheikine Y, Rocha VZ, Christen T, Shvartz E, Sukhova GK, etal. Hypoxia but not

inammation augments glucose uptake in human macrophages: Implications for imaging atherosclerosis with 18uorine-labeled 2-deoxy-D-glucose positron emission tomography. J Am Coll Cardiol. 2011;58:603–14.

74. Pedersen SF, Græbe M, Hag AM, Højgaard L, Sillesen H, Kjær A. (18)F-FDG imaging of

human atherosclerotic carotid plaques reects gene expression of the key hypoxia marker HIF-1α. Am J Nucl Med Mol Imaging. 2013;3:384–92.

75. Camici PG, Rimoldi OE, Gaemperli O, Libby P.Non-invasive anatomic and functional imag-

ing of vascular inammation and unstable plaque. Eur Heart J. 2012;33:1309–17.

76. Marnane M, Merwick A, Sheehan OC, Hannon N, Foran P, Grant T, etal. Carotid plaque

inammation on 18F-uorodeoxyglucose positron emission tomography predicts early stroke recurrence. Ann Neurol. 2012;71:709–18.

77. Rominger A, Saam T, Wolpers S, Cyran CC, Schmidt M, Foerster S, etal. 18F-FDG PET/CT

identies patients at risk for future vascular events in an otherwise asymptomatic cohort with neoplastic disease. J Nucl Med. 2009;50:1611–20.

78. Figueroa AL, Abdelbaky A, Truong QA, Corsini E, MacNabb MH, Lavender ZR, et al.

Measurement of arterial activity on routine FDG PET/CT images improves prediction of risk of future CV events. JACC Cardiovasc Imaging. 2013;6:1250–9.

79. Hawkins RA, Choi Y, Huang SC, Hoh CK, Dahlbom M, Schiepers C, etal. Evaluation of the

skeletal kinetics of uorine-18-uoride ion with PET.J Nucl Med. 1992;33:633–42.

80. Dweck MR, Chow MW, Joshi NV, Williams MC, Jones C, Fletcher AM, et al. Coronary

arterial 18F-sodium uoride uptake: a novel marker of plaque biology. J Am Coll Cardiol. 2012;59(17):1539–48.

81. Joshi NV, Vesey AT, Williams MC, Shah AS, Calvert PA, Craighead FH, et al. 18F-uoride

positron emission tomography for identication of ruptured and high-risk coronary atherosclerotic plaques: a prospective clinical trial. Lancet. 2014;383:705–13.

82. Costopoulos C, Brown AJ, Teng Z, Hoole SP, West NE, Samady H, etal. Intravascular ultra-

sound and optical coherence tomography imaging of coronary atherosclerosis. Int J Cardiovasc Imaging. 2016;32:189–200.

83. Mintz GS, Nissen SE, Anderson WD, Bailey SR, Erbel R, Fitzgerald PJ, etal. ACC Clinical

Expert Consensus Document on Standards for the acquisition, measurement and reporting of intravascular ultrasound studies: a report of the American College of Cardiology Task Force on Clinical Expert Consensus Documents (Committee to Develop a Clinical Expert Consensus Document on Standards for Acquisition, Measurement and Reporting of Intravascular Ultrasound Studies [IVUS]). J Am Coll Cardiol. 2001;37:1478–92.

84. Nair A, Margolis MP, Kuban BD, Vince DG.Automated coronary plaque characterisation with

intravascular ultrasound backscatter: exvivo validation. EuroIntervention. 2007;3:113–20.

85. Nair A, Kuban BD, Tuzcu EM, Schoenhagen P, Nissen SE, Vince DG. Coronary plaque

classication with intravascular ultrasound radiofrequency data analysis. Circulation. 2002;106:2200–6.

86. Rodriguez-Granillo GA, García-García HM, Mc Fadden EP, Valgimigli M, Aoki J, de Feyter

P, etal. In vivo intravascular ultrasound-derived thin-cap broatheroma detection using ultrasound radiofrequency data analysis. J Am Coll Cardiol. 2005;46(11):2038–42.

87. Stone GW, Maehara A, Lansky AJ, de Bruyne B, Cristea E, Mintz GS, etal. A prospective

natural-history study of coronary atherosclerosis. N Engl J Med. 2011;364:226–35.

F]-uorodeoxyglucose positron emission tomography.

K. Rana et al.

https://t.me/medicina_free

Mechanisms oftheVulnerable Atherosclerotic Plaque andImaging

88. Calvert PA, Obaid DR, O’Sullivan M, Shapiro LM, McNab D, Densem CG, etal. Association

between IVUS ndings and adverse outcomes in patients with coronary artery disease: the VIVA (VH-IVUS in Vulnerable Atherosclerosis) Study. JACC Cardiovasc Imaging. 2011;4:894–901.

89. Garcia-Garcia HM, Jang IK, Serruys PW, Kovacic JC, Narula J, Fayad ZA.Imaging plaques to

predict and better manage patients with acute coronary events. Circ Res. 2014;114:1904–17.

90. Kume T, Akasaka T, Kawamoto T, Okura H, Watanabe N, Toyota E, etal. Measurement of the

thickness of the brous cap by optical coherence tomography. Am Heart J. 2006;152:755 e1–4.

91. Tearney GJ, Yabushita H, Houser SL, Aretz HT, Jang IK, Schlendorf KH, etal. Quantication

of macrophage content in atherosclerotic plaques by optical coherence tomography. Circulation. 2003;107:113–9.

92. Nadkarni SK, Pierce MC, Park BH, de Boer JF, Whittaker P, Bouma BE, etal. Measurement

of collagen and smooth muscle cell content in atherosclerotic plaques using polarizationsensitive optical coherence tomography. J Am Coll Cardiol. 2007;49:1474–81.

93. Yabushita H, Bouma BE, Houser SL, Aretz HT, Jang IK, Schlendorf KH, etal. Characterization

of human atherosclerosis by optical coherence tomography. Circulation. 2002;106:1640–5.

94. Stefanadis C, Antoniou CK, Tsiachris D, Pietri P.Coronary atherosclerotic vulnerable plaque:

current perspectives. J Am Heart Assoc. 2017;6(3):e005543.

95. Tearney GJ, Regar E, Akasaka T, Adriaenssens T, Barlis P, Bezerra HG, et al. Consensus

standards for acquisition, measurement, and reporting of intravascular optical coherence tomography studies: a report from the International Working Group for Intravascular Optical Coherence Tomography Standardization and Validation. J Am Coll Cardiol. 2012;59:1058–72.

96. Sinclair H, Bourantas C, Bagnall A, Mintz GS, Kunadian V. OCT for the identication of

vulnerable plaque in acute coronary syndrome. JACC Cardiovasc Imaging. 2015;8:198–209.

97. Jang IK, Tearney GJ, MacNeill B, Takano M, Moselewski F, Iftima N, etal. In vivo char-

acterization of coronary atherosclerotic plaque by use of optical coherence tomography. Circulation. 2005;111:1551–5.

98. Raffel OC, Merchant FM, Tearney GJ, Chia S, Gauthier DD, Pomerantsev E, etal. In vivo

association between positive coronary artery remodelling and coronary plaque characteristics assessed by intravascular optical coherence tomography. Eur Heart J. 2008;29:1721–8.

99. Liu L, Gardecki JA, Nadkarni SK, Toussaint JD, Yagi Y, Bouma BE, etal. Imaging the sub-

cellular structure of human coronary atherosclerosis using micro-optical coherence tomography. Nat Med. 2011;17:1010–4.

100. Kashiwagi M, Liu L, Chu KK, Sun C-H, Tanaka A, Gardecki JA, etal. Feasibility of the

assessment of cholesterol crystals in human macrophages using micro optical coherence tomography. PLoS One. 2014;9(7):e102669.

101. Verjans JW, Osborn EA, Ughi GJ, Calfon Press MA, Hamidi E, Antoniadis AP, etal. Targeted

near-infrared uorescence imaging of atherosclerosis: clinical and intracoronary evaluation of indocyanine green. JACC Cardiovasc Imaging. 2016;9:1087–95.

102. Jaffer FA, Calfon MA, Rosenthal A, Mallas G, Razansky RN, Mauskapf A, et al. Two-

dimensional intravascular near-infrared uorescence molecular imaging of inammation in atherosclerosis and stent-induced vascular injury. J Am Coll Cardiol. 2011;57:2516–26.

103. Ughi GJ, Wang H, Gerbaud E, Gardecki JA, Fard AM, Hamidi E, etal. Clinical characteriza-

tion of coronary atherosclerosis with dual-modality OCT and near-infrared autouorescence imaging. JACC Cardiovasc Imaging. 2016;9:1304–14.

104. Zheng B, Mintz GS, McPherson JA, De Bruyne B, Farhat NZ, Marso SP, etal. Predictors of

plaque rupture within nonculprit broatheromas in patients with acute coronary syndromes: the PROSPECT study. JACC Cardiovasc Imaging. 2015;8:1180–7.

105. Narula J, Nakano M, Virmani R, Kolodgie FD, Petersen R, Newcomb R, etal. Histopathologic

characteristics of atherosclerotic coronary disease and implications of the ndings for the invasive and noninvasive detection of vulnerable plaques. J Am Coll Cardiol. 2013;61:1041–51.

106. Saba L, Anzidei M, Marincola BC, Piga M, Raz E, Bassareo PP, etal. Imaging of the carotid

artery vulnerable plaque. Cardiovasc Interv Radiol. 2014;37:572–85.

https://t.me/medicina_free

107. Underhill HR, Yuan C, Yarnykh VL, Chu B, Oikawa M, Polissar NL, etal. Arterial remodel-

ing in subclinical carotid artery disease. JACC Cardiovasc Imaging. 2009;2:1381–9.

108. Dweck MR, Puntman V, Vesey AT, Fayad ZA, Nagel E.MR imaging of coronary arteries and

plaques. JACC Cardiovasc Imaging. 2016;9:306–16.

109. Rogers IS, Nasir K, Figueroa AL, Cury RC, Hoffmann U, Vermylen DA, etal. Feasibility of

FDG imaging of the coronary arteries: comparison between acute coronary syndrome and stable angina. JACC Cardiovasc Imaging. 2010;3:388–97.

110. Gonzalo N, Garcia-Garcia HM, Regar E, Barlis P, Wentzel J, Onuma Y, etal. In vivo assess-

ment of high-risk coronary plaques at bifurcations with combined intravascular ultrasound and optical coherence tomography. JACC Cardiovasc Imaging. 2009;2:473–82.

111. Bezerra HG, Costa MA, Guagliumi G, Rollins AM, Simon DI. Intracoronary optical

coherence tomography: a comprehensive review clinical and research applications. JACC Cardiovasc Interv. 2009;2:1035–46.

112. Saam T, Ferguson MS, Yarnykh VL, Takaya N, Xu D, Polissar NL, et al. Quantitative

evaluation of carotid plaque composition by invivo MRI.Arterioscler Thromb Vasc Biol. 2005;25:234–9.

K. Rana et al.